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CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [ChIP-seq]

ABSTRACT: CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [ChIP-seq]

PROVIDER: PRJNA1037037 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26717700.fastq.gz	Fastqsanger.gz
	SRR26717701.fastq.gz	Fastqsanger.gz
	SRR26717702.fastq.gz	Fastqsanger.gz
	SRR26717703.fastq.gz	Fastqsanger.gz
	SRR26717704.fastq.gz	Fastqsanger.gz

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CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [1]

Project description:Cell plasticity theoretically extends to all possible cell types, but naturally decreases as cells differentiate, whereas injury-repair re-engages the developmental plasticity. Here we show that the lung alveolar type 2 (AT2)-specific transcription factor (TF), CEBPA, restricts AT2 cell plasticity in the mouse lung. AT2 cells undergo transcriptional and epigenetic maturation postnatally. Without CEBPA, both neonatal and mature AT2 cells reduce the AT2 program, but only the former reactivate the SOX9 progenitor program. Sendai virus infection bestows mature AT2 cells with neonatal plasticity where Cebpa mutant, but not wild type, AT2 cells express SOX9, as well as more readily proliferate and form KRT8/CLDN4+ transitional cells. CEBPA promotes the AT2 program by recruiting the lung lineage TF NKX2-1. The temporal change in CEBPA-dependent plasticity reflects AT2 cell developmental history. The ontogeny of AT2 cell plasticity and its transcriptional and epigenetic mechanisms have implications in lung regeneration and cancer.

2024-04-18 | GSE247130 | GEO

CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [scATAC-seq]

2024-04-16 | GSE264098 | GEO

CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [ChIP-seq]

2024-04-19 | GSE247271 | GEO

CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair

Project description:CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair

| PRJNA1037034 | ENA

CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [1]

Project description:CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [1]

| PRJNA1036384 | ENA

CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [scATAC-seq]

Project description:CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair [scATAC-seq]

| PRJNA1100986 | ENA

CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair.

| S-EPMC10760240 | biostudies-literature

CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-04-17 | GSE247272 | GEO

Release of Notch signaling coordinated by inflammation confers cross-compartment differentiation plasticity during alveolar regeneration.

Project description:While the acquisition of cellular plasticity in adult stem cells is essential for rapid restoration after tissue injury, little is known about the underlying molecular mechanisms governing this process. Here, we reveal that Notch signaling is a pivotal determinant conferring cross-compartment differentiation plasticity of airway secretory cells. Temporal Notch inhibition in secretory cells is required for alveolar differentiation upon injury, which is mediated by IL-1β-dependent modulation of Jag1/2 expression in ciliated cells. We also identify Fosl2/Fra2 as an essential transcription factor responsible for the regeneration of secretory cell-derived alveolar type 2 (sAT2) cells retaining distinct genetic/epigenetic signatures. We furthermore reveal that KDR/FLK-1+ human secretory cells display a conserved capacity to generate AT2 cells via Notch inhibition. Our results demonstrate that Notch signaling acts as a functional rheostat for fate decision of secretory cells during injury repair, proposing a new potential therapeutic target for human lung alveolar regeneration.

2021-09-08 | GSE154218 | GEO

Release of Notch signaling coordinated by inflammation confers cross-compartment differentiation plasticity during alveolar regeneration

Project description:While the acquisition of cellular plasticity in adult stem cells is essential for rapid restoration after tissue injury, little is known about the underlying molecular mechanisms governing this process. Here, we reveal that Notch signaling is a pivotal determinant conferring cross-compartment differentiation plasticity of airway secretory cells. Temporal Notch inhibition in secretory cells is required for alveolar differentiation upon injury, which is mediated by IL-1β-dependent modulation of Jag1/2 expression in ciliated cells. We also identify Fosl2/Fra2 as an essential transcription factor responsible for the regeneration of secretory cell-derived alveolar type 2 (sAT2) cells retaining distinct genetic/epigenetic features. We furthermore reveal that KDR/FLK-1+ human secretory cells display a conserved capacity to generate AT2 cells via Notch inhibition. Our results demonstrate that Notch signaling acts as a functional rheostat for fate decision of secretory cells during injury repair, proposing a new potential therapeutic target for human lung alveolar regeneration.

2021-09-08 | GSE153677 | GEO

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